Objectives To define, at the single cell level, the morphological changes that characterize retinal ganglion cell atrophy in eyes with experimentally elevated intraocular pressure (IOP), and to compare the time course of these neuronal changes with those that occur in the primary target of retinal axons, the dorsal lateral geniculate nucleus of the thalamus (LGN). Abstract Glaucoma is a leading cause of blindness. Clinically, most cases are characterized by elevated intraocular pressure (IOP), structural changes of the optic disc, and a loss of vision. Few data are available concerning the pattern of glaucomatous neuropathy that occurs within the retina and its central target, the dorsal lateral geniculate nucleus (LGN). The goal of this research is to define the temporal relation between the onset and progression of glaucoma measured clinically, and the atrophy of ganglion cells and LGN neurons. Elevated IOP is induced in rhesus monkeys using a non-invasive laser procedure. After 1-3 months of elevated IOP, the animals are anesthetized, enucleated, and perfused with formol saline. The retinae are isolated, placed in a chamber, and single retinal ganglion cells are stained intracellularly. The brains are embedded, sectioned, and cell size measurements are obtained from each LGN. Intracellular staining reveals abnormalities in the dendrites, but not necessarily the axons and somata, of ganglion cells following as little as 2-3 weeks of elevated IOP. In the LGN, little difference in cell body size is seen following 2-3 weeks of elevated IOP, while by 6 months there is approximately a 50% reduction in the cross-sectional areas of neurons receiving input from the glaucomatous eye. These data suggest 1) that structural changes at the level of the cell body represent late, and not early, stages of glaucoma-related ganglion cell death, 2) that the onset of pressure-induced retinal ganglion cell degener ation occurs earlier than previously thought based on cell soma studies, and 3) that retinal ganglion cell degeneration in glaucoma is not necessarily a retrograde effect that is secondary to damage to the optic nerve. These data concerning the temporal pattern of glaucomatous retinal ganglion cell atrophy are important for the development of early detection and treatment strategies aimed at promoting retinal ganglion cell survival. Key words retina, ganglion cells, glaucoma, degeneration, intraocular pressure